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Transcript profiling of the immunological interactions between Actinobacillus pleuropneumoniae serotype 7 and the host by dual RNA-seq

BACKGROUND: The complexity of the pathogenic mechanism underlying the host immune response to Actinobacillus pleuropneumonia (App) makes the use of preventive measures difficult, and a more global view of the host-pathogen interactions and new insights into this process are urgently needed to reveal...

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Autores principales: Li, Ping, Xu, Zhiwen, Sun, Xiangang, Yin, Yue, Fan, Yi, Zhao, Jun, Mao, Xiyu, Huang, Jianbo, Yang, Fan, Zhu, Ling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5596872/
https://www.ncbi.nlm.nih.gov/pubmed/28899359
http://dx.doi.org/10.1186/s12866-017-1105-4
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author Li, Ping
Xu, Zhiwen
Sun, Xiangang
Yin, Yue
Fan, Yi
Zhao, Jun
Mao, Xiyu
Huang, Jianbo
Yang, Fan
Zhu, Ling
author_facet Li, Ping
Xu, Zhiwen
Sun, Xiangang
Yin, Yue
Fan, Yi
Zhao, Jun
Mao, Xiyu
Huang, Jianbo
Yang, Fan
Zhu, Ling
author_sort Li, Ping
collection PubMed
description BACKGROUND: The complexity of the pathogenic mechanism underlying the host immune response to Actinobacillus pleuropneumonia (App) makes the use of preventive measures difficult, and a more global view of the host-pathogen interactions and new insights into this process are urgently needed to reveal the pathogenic and immune mechanisms underlying App infection. Here, we infected specific pathogen-free Mus musculus with App serotype 7 by intranasal inoculation to construct an acute hemorrhagic pneumonia infection model and isolated the infected lungs for analysis of the interactions by dual RNA-seq. RESULTS: Four cDNA libraries were constructed, and 2428 differentially expressed genes (DEGs) of the host and 333 DEGs of App were detected. The host DEGs were mainly enriched in inflammatory signaling pathways, such as the TLR, NLR, RLR, BCR and TCR signaling pathways, resulting in large-scale cytokine up-regulation and thereby yielding a cytokine cascade for anti-infection and lung damage. The majority of the up-regulated cytokines are involved in the IL-23/IL-17 cytokine-regulated network, which is crucial for host defense against bacterial infection. The DEGs of App were mainly related to the transport and metabolism of energy and materials. Most of these genes are metabolic genes involved in anaerobic metabolism and important for challenging the host and adapting to the anaerobic stress conditions observed in acute hemorrhagic pneumonia. Some of these genes, such as adhE, dmsA, and aspA, might be potential virulence genes. In addition, the up-regulation of genes associated with peptidoglycan and urease synthesis and the restriction of major virulence genes might be immune evasion strategies of App. The regulation of metabolic genes and major virulence genes indicate that the dominant antigens might differ during the infection process and that vaccines based on these antigens might allow establishment of a precise and targeted immune response during the early phase of infection. CONCLUSION: Through an analysis of transcriptional data by dual RNA-seq, our study presents a novel global view of the interactions of App with its host and provides a basis for further study. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12866-017-1105-4) contains supplementary material, which is available to authorized users.
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spelling pubmed-55968722017-09-15 Transcript profiling of the immunological interactions between Actinobacillus pleuropneumoniae serotype 7 and the host by dual RNA-seq Li, Ping Xu, Zhiwen Sun, Xiangang Yin, Yue Fan, Yi Zhao, Jun Mao, Xiyu Huang, Jianbo Yang, Fan Zhu, Ling BMC Microbiol Research Article BACKGROUND: The complexity of the pathogenic mechanism underlying the host immune response to Actinobacillus pleuropneumonia (App) makes the use of preventive measures difficult, and a more global view of the host-pathogen interactions and new insights into this process are urgently needed to reveal the pathogenic and immune mechanisms underlying App infection. Here, we infected specific pathogen-free Mus musculus with App serotype 7 by intranasal inoculation to construct an acute hemorrhagic pneumonia infection model and isolated the infected lungs for analysis of the interactions by dual RNA-seq. RESULTS: Four cDNA libraries were constructed, and 2428 differentially expressed genes (DEGs) of the host and 333 DEGs of App were detected. The host DEGs were mainly enriched in inflammatory signaling pathways, such as the TLR, NLR, RLR, BCR and TCR signaling pathways, resulting in large-scale cytokine up-regulation and thereby yielding a cytokine cascade for anti-infection and lung damage. The majority of the up-regulated cytokines are involved in the IL-23/IL-17 cytokine-regulated network, which is crucial for host defense against bacterial infection. The DEGs of App were mainly related to the transport and metabolism of energy and materials. Most of these genes are metabolic genes involved in anaerobic metabolism and important for challenging the host and adapting to the anaerobic stress conditions observed in acute hemorrhagic pneumonia. Some of these genes, such as adhE, dmsA, and aspA, might be potential virulence genes. In addition, the up-regulation of genes associated with peptidoglycan and urease synthesis and the restriction of major virulence genes might be immune evasion strategies of App. The regulation of metabolic genes and major virulence genes indicate that the dominant antigens might differ during the infection process and that vaccines based on these antigens might allow establishment of a precise and targeted immune response during the early phase of infection. CONCLUSION: Through an analysis of transcriptional data by dual RNA-seq, our study presents a novel global view of the interactions of App with its host and provides a basis for further study. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12866-017-1105-4) contains supplementary material, which is available to authorized users. BioMed Central 2017-09-12 /pmc/articles/PMC5596872/ /pubmed/28899359 http://dx.doi.org/10.1186/s12866-017-1105-4 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Li, Ping
Xu, Zhiwen
Sun, Xiangang
Yin, Yue
Fan, Yi
Zhao, Jun
Mao, Xiyu
Huang, Jianbo
Yang, Fan
Zhu, Ling
Transcript profiling of the immunological interactions between Actinobacillus pleuropneumoniae serotype 7 and the host by dual RNA-seq
title Transcript profiling of the immunological interactions between Actinobacillus pleuropneumoniae serotype 7 and the host by dual RNA-seq
title_full Transcript profiling of the immunological interactions between Actinobacillus pleuropneumoniae serotype 7 and the host by dual RNA-seq
title_fullStr Transcript profiling of the immunological interactions between Actinobacillus pleuropneumoniae serotype 7 and the host by dual RNA-seq
title_full_unstemmed Transcript profiling of the immunological interactions between Actinobacillus pleuropneumoniae serotype 7 and the host by dual RNA-seq
title_short Transcript profiling of the immunological interactions between Actinobacillus pleuropneumoniae serotype 7 and the host by dual RNA-seq
title_sort transcript profiling of the immunological interactions between actinobacillus pleuropneumoniae serotype 7 and the host by dual rna-seq
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5596872/
https://www.ncbi.nlm.nih.gov/pubmed/28899359
http://dx.doi.org/10.1186/s12866-017-1105-4
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